Fiziologia somnului

SOMNUL = componenta esentiala a integritatii si functionarii normale a creierului si intregului

organism al fiintelor umane si animale

SOMNUL = stare activa a creierului, cu propriile sisteme de retele neuronale functionale si

mecanisme de control a homeostaziei specifice extrem de complexe

SOMNUL = componenta inseparabila a ciclurilor somn-veghe

Somnul = o stare fiziologica de intrerupere a activitatii de veghe constiente,

cand creierul este relativ mai reactiv la stimuli interni decat la stimuli externi

- alternanta somn-veghe are o ciclicitate predictibila

( diferenta majora fata de starile patologice de pierdere a constientei )

- creierul isi scade gradual responsivitatea la stimuli vizuali, auditivi si alti

stimuli din mediu tranzitia catre somn ( stadiul I de somn NREM )

Proiectiile eferente ale FR trunchiului cerebral

1. rostral spre creierul bazal anterior ( forebrain)

2. caudal spre maduva spinarii

3. spre sistemele motorii & de reglare interna

Components of the consciousness system

 Somnul urmeaza un ritm circadian - cu periodicitate reglata genetic independent de un ceas
biologic intrinsec ( in relatie cu factori-trigger externi: lumina, intuneric, orele zilei,
modalitatile de activitate, orele meselor, etc.)

Cand fiinta umana este privata de acesti factori-cheie si supusa unui nivel constant de
iluminare, ciclul somn-veghe se alungeste la cca. 24,5 ore

CEASUL BIOLOGIC CIRCADIAN ( la om )

Ceasul biologic principal la mamifere nc. suprachiasmatic ( SCN ) din h-talamusul

rostral ( sincronizeaza activitatile diurne )

Leziuni din SCN pierderea organizarii circadiene

Proiectii directe din retina

la om, cel mai puternic agent de sincronizare: LUMINA

alternanta lumina / intuneric: organizeaza ritmul biologic

nevoia de adormire

momentul trezirii

Informatii aferente multiple de la caile celorlalti stimuli externi reglatori

Reglarea ritmului veghe somn

Interactiune coordonata intre circuitele neuronale de control ale:

A. reglarii starii de veghe (stimuleaza activarea corticala & trezirea comportamentala )

nn. Ach-ergici din: TRUNCHI CEREBRAL si CREIERUL ANTERO-BAZAL

 nn. monoaminergici (NA, Hys-NH2, 5-HT2 ) din: TRUNCHIUL CEREBRAL si
HIPOTALAMUSUL POSTERIOR

nn. orexigenici ( hipocretina ) din HIPOTALAMUSUL LATERAL

( distrugerea neuronilor orexinici narcolepsia ! )

A. reglarii somnului

inhibitia /disfacilitarea sistemelor de trezire prin:

cell. ARIA PREOPTICA VENTRAL-LATERALA ( VLPO )

galanina, GABA

nc. PREOPTIC MEDIAN ( MnPN )

GABA

Neuronii preoptici se activeaza in timpul somnului si se proiecteaza in hipotalamusul posterior si

trunchiul cerebral rostral ( INHIBITIE )

( pattern de descarcare reciproc celui din sistemele de veghe )

Both homeostatic factors (factor S) and circadian factors (factor C) interact to determine the timing
and quality of sleep

The propensity to fall asleep varies throughout the day and depends upon both time since the last
sleep period (process S) and circadian factors (process C):

- the longer the time since the last sleep period, the greater will be

process S;

- its propensity will be modulated by process C

The circadian pressure to sleep:

- is greatest at ~2 am with a secondary peak at ~2 pm.

- it is least at ~6 am and ~6 pm.

OREXINELE ( HIPOCRETINELE )
Orexins or hypocretins, which are produced by a small group of neurons in the hypothalamus
and whose actions are mediated by two types of receptors: OX1R and OX2R

Orexinergic neurons are projected widely into a number of brainstem, cortical and limbic
regions

They have been related with the mechanisms that enable regulation of the sleep-wake cycle,
the ingestion of food and drink, and some particular types of learning

Further research will help to determine the functioning of orexinergic neurons and the
interaction between the systems that regulate emotion, energetic homeostasis and the
reward mechanisms, on the one hand, and the systems that regulate the sleep-wake cycle on
the other

STRUCTURA GENERALA A
SOMNULUI
2 componente fundamentale ale somnului:

non-REM ( NREM )

Clasic: 4 stadii de profunzime: I, II ( somn superficial ), III, IV ( SWS )

Clasificarea actuala AASM: N1, N2, N3

REM

Diferente majore NREM / REM:

- circuite neuronale activate

- relatia creier / mediul exterior si intern (controlul homeostaziei sistemice,

activitatii motorii si receptivitatii informatiilor din afara SNC )

- tipul de activitate biochimica in metabolismul si comunicarea interneuronala

* NREM: activitate mentala minima / absenta

* REM: activitate corticala intensa

- activitatea electrica a creierului EEG

Sleep is divided into a 90 minute cycle of NREM sleep and REM sleep
 This cycle is repeated 3-6 times during the night

Generally, a night of sleep begins in NREM and progresses through deeper NREM stages
(stages 2, 3, and 4 using the classic definitions, or stages N2 and N3 using the updated
definitions) before the first episode of REM sleep occurs approximately 80 to 100 minutes
later

As the sleep cycle progresses through the night there is less stage N3 NREM sleep and more
REM sleep ( more REM sleep on towards morning, which explains why when you awaken in
the morning, you generally awaken from a dream )

Stage 1 sleep is a very light stage of sleep with a low arousal threshold. It generally lasts for
less than 10 minutes, at sleep onset. During this stage, the EEG shows alpha activity

During stage 2 sleep, which accounts for 50 percent of total sleep time, the EEG shows low-
voltage activity

EEG:

low-voltage activity

the frequency is mixed, but slowing

advancement to Stage 2 begins when K-complexes and sleep spindles that last
at least 0.5 second, on a background of theta waves

sleep spindles: high-frequency bursts (12-16 Hz) of electrical activity

( hypnotic agents have been shown to increase the density of sleep spindles )

the K-complex: the most prominent feature of Stage 2 and may be elicited by
an auditory stimulus.

Muscle tone persists during Stage 2

Eye movements during Stage 2 are generally slow or absent, although they may
reappear for short intervals

 The induction of SWS ( S3-S4/ N3) is associated with the secretion of -aminobutyric acid
(GABA) from basal forebrain neurones

( benzodiazepines and barbiturates, which act through

stimulation of GABA receptors in the CNS, induce sleep

or anesthesia )

ARHITECTURA SOMNULUI
An EEG pattern of 20%-50% high-amplitude, low frequency (2 Hz) delta waves signifies the
onset of Stage 3 ( N3). Sleep spindles and K-complexes can still be identified

Progression to Stage 4 is defined as an EEG pattern of more than 50% high-amplitude, low-
frequency waves ( elta )

Muscle tone and eye movement are greatly diminished or absent during Stages 3 and 4 ( N3 )

American Academy of Sleep Medicine (AASM) terminology uses the term N for NREM sleep
stages and R for REM sleep stages:

N1 and N2 are used instead of stage 1 and stage 2

N3 is used to indicate the sum of stage 3 and stage 4 (slow-wave sleep SWS )

In Phase N1: alpha waves with frequencies of 8-13 Hz change to theta waves with frequencies
of 4-7 Hz

Phase N2: marked with the advent of sleep spindles that range from 11-16 Hz and K-
complexes

Phase N3 (deep sleep): EEG pattern of 20%-50% high-amplitude (>75 V), low-frequency
(2 Hz) delta waves

In starea de veghe: Ach, Hys-NH2, NA ( din trunchiul cerebral & hipotalamus ) au

efect activator asupra neuronilor talamo-corticali, blocand hiperpolarizarea prin canalele de
K+

In stad.N2 NREM: inhibitia sincrona produsa de GABA: abundenta de fusuri de somn

In somnul SWS ( NREM-N3 ):

scaderea Ach ( dezinhibitia nc. reticular talamici ), prin reducerea depolarizarii

SRAA ( in somnul precoce ) permite un raspuns de tip burst-mode dependent
de un prag scazut al canalelor lente de Ca++ ( descarcari de serii repetitive pe
fond de hiperpolarizare )
REM
A specific subset of cholinergic neurons within the pontine reticular formation seems to dictate
the nature of REM sleep: during SWS, these cholinergic neurons also suppress the activities of
aminergic neurons

The transition from SWS to REM sleep can be partially attributed to a reduction in the
suppression of aminergic neurons

REM sleep usually is not divided into stages

For research purposes:

tonic (parasympathetically driven state ) REM sleep ( with no eye movements )

phasic (sympathetically driven state ) REM sleep ( with eye movements that tend to
occur in clusters )

The most commonly used marker of REM sleep phasic activity in human beings is the bursts of
rapid eye movements

Muscle twitches and cardiorespiratory irregularities often accompany the sympathetically

driven phasic REM bursts

1. The MENTAL ACTIVITY of human REM sleep is associated with DREAMING, based on vivid
dream recall reported after approximately 80% of arousals from this state of sleep

2. Inhibition of spinal motor neurons by brainstem mechanisms mediates SUPPRESSION OF

POSTURAL MOTOR TONUS in REM sleep

( postsynaptic inhibition of motor neurons and membrane hyperpolarization; in subjects with

pontine damage, REM without atonia can occur these patients physically enact the events of their
dreams )

A shorthand definition of REM sleep:

AN ACTIVATED BRAIN IN A PARALYZED BODY

Classic EEG features of REM sleep include high-frequency, irregular waveforms and the
absence of K-complexes, sleep spindles, and low-frequency waveforms

The irregular waveforms unique to REM sleep have a sawtooth appearance and are present
in bursts lasting up to 5 seconds

In terms of EEG readings, REM sleep most closely resembles the waking state

REM sleep is also characterized by:

EEG activation

muscle atonia

episodic bursts of rapid eye movements

 diminished or absent deep tendon reflexes

irregular breathing in both frequency and tidal volume

poikilothermia ( cells in the preoptic/anterior hypothalamus which control

thermoregulation cease firing )

penile tumescence

increased variability in cardiac rhythm

cerebral blood flow is also high during REM sleep

Neurotransmitters
Simplistic
Wake
high monoaminergic
high cholinergic
orexin ( hypocretin )
NREM
low monoaminergic
low cholinergic
REM
low monaminergic
high cholinergic
Monoaminergic: dopamine, serotonin, norepinephrine, hystamine

PHYSIOLOGICAL CHANGES
DURING SLEEP
Cardiovascular

* During NREM, there is an overall reduction in heart rate, cardiac output and blood pressure
( dip), due to a general vasodilation
 * During REM sleep, there are variations in blood pressure and heart rate, but overall the
rates are increased, especially during the phasic events of REM sleep, probably due to a generalized
vasoconstriction seen in the skeletal muscles during phasic REM sleep

* Cardiac output is generally decreased during all sleep phases

* Cerebral blood flow (CBF) increases above the level of resting wakefulness during tonic REM
sleep and is even greater during phasic REM sleep

* Cerebral metabolic rate, oxygen consumption and neuronal discharge rate are reduced
during NREM sleep but increased above resting values during REM sleep

The autonomic nervous system shows a general decrease in sympathetic tone and an
increase in parasympathetic tone, except in phasic REM sleep.

Respiration
* Overall, there is slight hypercapnia, a decrease in total ventilation, and a decreased
sensitivity to inspired CO2

* During NREM there is a slight hypoventilation ( relaxation of upper airway muscles, as well
as a decrease in the firing of inspiratory neurons, which show a decreased sensitivity to stimuli )

* PCO2 levels raise while Po2 levels fall

* During NREM sleep, breathing is under chemical and mechanical feedback control

* During REM there is an overall higher and variable respiratory rate ( it may be driven by higher
cortical control, which may explain the variable rate )

NERVOUS SYSTEM DURING SLEEP

During NREM sleep there is a reduced discharge rate and reduced brain metabolism (there is
an active inhibition of the reticular activating system )
 During REM sleep, many parts of brain (visual cortex, limbic lobe) show increased firing rate
and metabolism

Brain transection studies have shown that the pons is necessary and sufficient to generate the
basic phenomena of REM sleep

During NREM sleep, brain transection studies have shown that the pons is
necessary and sufficient to generate the basic phenomena of REM sleep
During NREM sleep, there is an increase in parasympathetic activity similar to relaxed
wakefulness; sympathetic drives remain at about the same level as during relaxed
wakefulness

During tonic REM sleep, parasympathetic activity remains about the same as during NREM
sleep, but sympathetic activity decreases, resulting in an overall predominance of
parasympathetic activity

However, during phasic REM sleep, both sympathetic and parasympathetic activity increase;
sympathetic activation is generally favored

Overall, there is a reduced discharge rate and reduced brain metabolism during NREM

***RELATIA INERVATIEI CHOLINERGICE /

STAREA VIGILA si SOMNUL / MEMORIA
Eliberarea corticala a Ach:
crescuta in timpul starii de veghe
maxima si exclusiva in somnul REM
minima in somnul SWS

A. Starea de veghe: Ach creste selectivitatea raspunsului neuronal la informatia noua,

favorizand retinerea ei ( encodarea )
B. NREM: influenta benefica asupra memoriei declarative !
reactivarea achizitiilor mnestice recente (replay) in circuitele hipocampice,
NECESARA pentru transferul si integrarea lor in retelele celulare neocorticale ( corelate cu
prezenta in std.2 NREM pe EEG a fusurilor de somn si oscilatiilor lente, mai abundente dupa
procesul de invatare declarativa )
activitatea NA in absenta activitatii Ach permite consoloidarea memoriei de
lunga durata in retelele neocorticale, prin facilitarea activitatii metabolice
celulare ( sinteze proteice: LTP de lunga durata )
reflecta activitatea neocorticala si talamica ( ncc. anteriori ):
inversarea fluxului informational ( hipocamp neocortex )
 necesita reducerea stimularii Ach si cortizolice ( implicatii pentru AD,
apneea de somn, nerespectarea orelor de somn, s.a.)

C. Somnul REM:
* consolidarea memoriei procedurale
* consolidarea memoriei declarative cu continut emotional bogat !
Mecanisme asemanatoare ca pentru memoria declarativa, dar implica activarea de
catre hipocamp a STRIATULUI ( memoria abilitatilor motorii )
replay in circuitele subcorticale hipocampic-striate
participarea circuitelor cerebeloase

Generalizarea dependenta de somn

Proces fiziologic care permite unui organism sa realizeze o constructie mintala noua,
adaptativa pe baza unei experiente anterioare si sa raspunda astfel mai flexibil la
informatii noi din mediul extern, altul decat cel in contextul caruia s-a realizat procesul
mnestic initial
ameliorarea functiei executive
creativitatea
introspectia
performanta intelectuala mai buna
performante comportamentale mai bune
Generalizarea dependenta de somn
pare legata de fenomenele de replay ( inainte si mai ales inapoi ) de la nivelul
hipocampului, din cursul somnului mai ales REM, dar si in SWS ( roluri
secventiale )
Activitatea cerebrala din somnul REM ( talamus, girus cingulat anterior, operculul
parietal, complexul amigdalian ) asociata cu activitate imaginativa vie ( visul ) si
inhibitia quasi-totala cu mediul extern ( senzorial & comportamental, motor )
Trezirea din somnul NREM: subiectul relateaza aspecte corelate explicit cu activitatea
sa mnestica recenta ( corelatie cu activarea reg. parahipocampice in somnul NREM,
implicata in codarea mnestica )
Somnul REM si NREM au roluri secventiale in realizarea si consolidarea memoriei,
concomitent cu odihna fizica si refacerea metabolica sistemica

CRESTE PERFORMANTA IN STAREA DE VEGHE
Activitatea endocrina in cursul somnului

A. Activitatea hormonala dependenta de somn ( in ansambu ) ( ex.: prolactina )

B. Activitatea hormonala in relatie cu un stadiu particular de somn ( ex.: STH/ GH )

C. Activitatea hormonala independenta de alternanta veghe/ somn ( ex.: ACTH, cortizol )

Activitatea hormonala depine de interactiunea a mai multi factori, intre care si mai multe cicluri
biologice care interactioneaza:

- veghe/ somn

- cicluri circadiene

- cicluri infradiene (frecventa < 1/ zi; perioada > 24h)

- cicluri ultradiene (frecventa > 1/zi; perioada < 24 h, dar > 1h)

PROLACTINA

nivele scazute in conditii bazale, in starea de veghe relatie de tip circadian

cresteri usoare in cursul somnului

privarea de somn: atenueaza secretia de PRL

decalarea orelor de somn: decalarea ciclurilor secretorii de PRL

modificarea fusului orar: adaptarea ritmului PRL necesita un decalaj de timp

TSH

variatii mari intra- si interindividuale

date contradictorii, functie de studii:

concentratii crescute in timpul somnului

peak secretor inainte de adormire, scadere progresiva in cursul somnului de noapte

concentratii nocturne crescute in cursul privarii de somn

HORMONUL DE CRESTERE ( STH/ GH )

concentratie scazuta in cursul starii de veghe, in cursul zilei

exceptie episoadele secretorii declansate de:

ingestia de alimente

efortul muscular

secretia incepe imediat dupa adormire; este maxima in stad. N3 ( SWS std. III-IV )
 somnul REM influenta inhibitorie

diferente functie de sex si varsta:

barbati tineri: 3 episoade ( in medie ) in cursul somnului de noapte

femei: variabilitate mai mare, influenta importanta a ciclului menstrual

secretia totala dimnua cu inaintarea in varsta ( se pastreaza secretia maxima in

cursul somnului, la orice varsta !)

ALTI HORMONI ADENOHIPOFIZARI ( TSH, LH, ACTH )

concentratia scade la trecerea din somnul NREM spre somnul REM

SISTEMUL RENINA ANGIOTENSINA ALDOSTERON

Secretia de RENINA are un ritm circadian

nivelul cel mai scazut ( in pozitie culcat ): mijlocul dupa-amiezii

nivelul maxim: spre finalul noptii

fluctuatii in cursul ciclurilor NREM/ REM:

declin la debutul fiecarei faze REM

eliberare crescuta la trecerea din REM catre NREM, si la trezire

Secretia de ALDOSTERON are ritm circadian asemanator

oscilatii nocturne cu ritm de 90 min, dar independent de ciclurile de somn

nivelele de aldosteron le reflecta pe cele de renina cu un decalaj de cca. 20 min

inhibitia reninei pe cale farmacologica ( terapia anti-HTA ): profilul secretor al

aldosteronului urmeaza dinamica ACTH

ACTH si CORTIZOL

evolutie in mare masura paralela, dar nu identica

secretie maxima: dimineata devreme ( incepe relativ rapid in jurul orelor 04:00 a.m. )

secretia scade in cursul zilei nivelul cel mai scazut: la sfarsitul serii

profilul secretor nu este influentat de somn

MELATONINA

secretie ritmata de alternanta lumina / intuneric, dar neinfluentata de somn

secretie minimala in cursul zilei

debutul secretiei continue: inainte de adormire maximum in cursul noptii

TESTOSTERONUL

lipsa de interactiune cu somnul ( studii putine )

HORMONUL LUTEINIZANT ( LH )
 secretie neifluentata de ritmul somn/ veghe si fazele de somn

Rezistenta la insulina si ritmul circadian

Toleranta la glucoza mai scazuta in cursul serii si noptii

influenta ciclurilor somn/ veghe si lipsa de aport alimentar/ hranire: nu este bine
elucidata

nerespectarea programului de lucru ( lucrul in cursul noptii ) = factor de risc pentru

diabetul zaharat (!)

Studii recente:

toleranta la glucoza este semnificativ mai scazuta seara ( orele 20:00 ) decat
dimineata ( orele 08:00 ), independent de ciclul comportamental

seara, secretia de insulina pancreatica ( celulele ) scade cu cca. 27%

discordanta intre ciclul somn/ veghe si ciclul comportamental altereaza

toleranta la glucoza (!)

inversarea ciclului comportamental cu 12 ore, creste glicemia postprandiala

( scade toleranta la glucoza = creste rezistenta la insulina )

probabil scade sensibilitatea receptorilor la insulina

Activitatea neurocognitiva si circuitele neuronale

Procesele neurocognitive oscilatii sincrone ale activitatii neuronale in zone cerebrale
interconectate intre ele la distanta, dar implicate in acelasi proces [ v. conectivitatea retelelor
neuronale in repaus ( resting state) & activate de activitati specifice ( task-specific )]
Rolul somnului asupra functiilor neurocognitive
Privarea de somn altereaza functiile neurocognitive

Fiecare stadiu de somn asociat cu efecte specifice asupra functiilor cognitive

in particular: memoria, invatarea, functia executiva, atentia complexa

Somnul permite consolidarea selectiva a memoriei si minimizeaza riscul dezorganizarii

sale prin intreruperea achizitiilor continue

Somnul are efecte benefice si asupra altor functii cognitive si mintale derivate:

creativitate, capacitatea de introspectie, functia executiva

Istorie:

1959 ( ultimul experiment uman de privare de somn ):

Peter Tripp - privare de somn 201 ore ( incinta de sticla in New Yorks Times Square )

dupa 72 ore: halucinatii, depresie, incoerenta

Insomnia fatala familiala ( boala prionica )

pierdere progresiva a capacitatii de a dormi deteriorare cognitiva

progresiva dementa deces

Dupa exercitii de training cognitiv cresteri spontane ale activitatii REM

activitatea PGO ( origine: nc.subcoeuleus, propagare: SRRA medial; tinta: GLU in

creierul bazal anterior proiectie in hipocamp, amigdala, cortex occipital ) - crescuta
in relatie cu training-ul cognitiv
 activitatea PGO ~ corelata cu retentia informatiilor noi

PGO induc activitate theta in hipocamp

neuronii din hipocamp care au fost anterior activi in starea de veghe se reactiveaza
in REM

( replay al activitatii din starea de veghe ) concomitent cu activitatea theta si inductia LTP/ LTD

Ach permite activitatea theta in hipocamp in starea de veghe si in somnul REM ( mai
mult decat in veghe )

disruptia activitatii Ach in REM altereaza retentia informatiilor

Hipocampul = sediul stocarii temporare a informatiilor noi & al memoriei asociative

informatii noi depotentierea ( LTD) informatiilor vechi din hipocamp cu acelasi tip de
continut

DEPOTENTIEREA - facilitata de absenta activitatii NA ( care faciliteaza LTP ) si

5-HT

Somnul REM:

carcteristicile electrofiziologice si biochimice asociate cu ambele procese,

bidirectionale ale neuroplasticitatii: LTP si LTD

undele ascutite PGO

sincronismul theta

nivelul minimal de monoamine biogene ( NA faciliteaza fen. feed-back in

neocortex )

nivelul Ach maximal ( corelat cu act. theta in hipocamp, reducerea trimiterii de

informatii din hipocamp spre neocortex )

transcriptia crescuta intraneuronal a genelor legate de plasticitate

mediu neuronal care permite remodelarea sinaptica ( mai ales in hipocamp )

rol particular in consolidarea si modularea memoriei emotionale & memoriei

procedurale

consolidarea memoriei declarative cu un continut emotional bogat

privarea de somn REM inhiba inducerea LTP si mentinerea informatiei

privarea prelungita de somn REM ( ore ) scade capacitatea de memorare si

neurogeneza legata de invatare in girusul dentat ( hipocampic )

IRMf: activitatea hipocampului este drastic redusa dupa o noapte de privare de somn
total

Somnul NREM - SWS:

 consolidarea memoriei: transferul informatiilor din hipocamp ( encodarea memoriei
prin LTP ) in arii neocorticale specifice ( stocarea pe termen indelungat )

undele lente permit reactivarea off-line a neuronilor implicati in procesul de

invatare sau memorare ( encodare ) de o maniera accelerata si condensata in timp +
concomitent permite si fenomenul LTD in sinapsele care au fost doar slab reactivate
( stergerea altor informatii ) => stabilizarea sinapselor ( unele sunt stabilizate-LTP ,
altele dezactivate - LTD )

sintezele proteice ( esentiale pentru LTP de lunga durata, initiat in REM ) sunt foarte
active

=> consolidarea memoriei

Experimental: la trezire, realizarea activitatilor dependente de zonele de cortex cu activitate de

unde lente in cursul SWS, este mult mai performanta

Somnul NREM stad.2:

fusurile de somn: se coreleaza cu eficienta invatarii in starea de veghe

generate de nc. reticular talamic cell.corticale oscileaza in fusuri ( 11-16

Hz )

nu apar in prezenta NA ( l.coeruleus - inactiv inainte de aparitia fusurilor de

somn, devine activ intens la sfarsitul fiecarui fus de somn consolidarea
memoriei de novo )

5-HT-NH2 si Ach scazute in talamus ( mediu biochimic ~ REM, dar fara

cresterea Ach )

hipocampul determina acelasi tip de reorganizare sinaptica birectionala in

cortexul prefrontal in NREM-N2 ~ in REM

Episoadele scurte de trezire off-line linistita din cursul somnului:

intercalarea informatiilor noi, alaturi de cele vechi in afara stimularii senzoriale

directe

Somnul NREM stad. 2:

fusurile de somn

incetarea activitatii continue NA urmata de descarcari ale neuronilor NA, in acelasi

timp cu reactivarea hipocampica si corticala

creste plasticitatea sinaptica

permite plasticitatea sinaptica bidirectionala ( LTP / LTD ) in arii neocorticale tinta

 SOMNUL NREM N3 ( activitate EEG tip delta )

reactivare neuronala in faza cu activitatea lenta tip delta

sinteza intracelulara ( neuron, glie ) crescuta de proteine

nivel Ach scazut

faciliteaza conversia LTP precoce in LTP de lunga durata ( nu se asociaza cu activarea

genelor de reactivitate precoce, precum in LTP precoce )

poate reduce forta circuitelor corticale, mai putin stimulate in reactivitarea delta
( stergere selectiva de informatii: uitarea este necesara pentru o memorie mai
performanta )